Alzheimer’s is ranked as the 6th leading cause of death in the United States, and mainly presented as neurodegeneration. In order to begin to understand its physiology, the specific role of proteins in neurodegeneration, LRP1 and AQP4, need to be studied. This study tested the effect of using the CRISPR-Cas9 system to overexpress the LRP1 and AQP4 proteins, associated with transport of materials and waste across the cell membrane, in Caenorhabditis elegans to assess effects on neurodegeneration, such as chemosensation, size, and average speed phenotypes. I hypothesized that combinatorial overexpression of AQP4 and LRP1 would have the greatest effect on reducing neurodegeneration. I tested chemosensory behavior using a chemotaxis test, revealing a decrease in neurodegeneration when both LRP1 and AQP4 were overexpressed. The size of the C. elegans did not change, but the speed increased in the strain expressing amyloid beta in the muscle, suggesting that a decrease in amyloid beta allowed muscles more room to contract. These results support our hypothesis and show that the overexpression of LRP1 and AQP4 proteins decrease neurodegeneration and allow C. elegans to preserve their olfactory retention. This study will help demonstrate the role of LRP1 and AQP4 in Alzheimer’s and determine whether they benefit the system once they are overexpressed.